Dysfunctional Coagulation in COVID-19: From Cell to Bedside.
Jie WangArdan M SagunerJiaqi AnYuye NingYang YanGuo-Liang LiPublished in: Advances in therapy (2020)
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19), which can induce multisystem disease. Human angiotensin-converting enzyme 2 (ACE2) widely expressing in arterial and venous endothelial cells and arterial smooth muscle cells has been identified as a functional receptor for SARS-CoV-2. Dysfunction of ACE2 leads to abnormal activation of the renin-angiotensin system and a systemic endotheliitis that may relate to abnormal coagulation and sepsis. Meanwhile, innate immune response and inflammation activation participate in dysfunctional coagulation. Previous research indicated that dysfunctional coagulation was one of the important risk factors accountable for a high risk of severe disease and death in patients with COVID-19. Understanding the possible mechanisms of dysfunctional coagulation and appropriate anticoagulation therapeutic strategies are important to prevent disease deterioration and reduce fatality rates during the ongoing COVID-19 pandemic.
Keyphrases
- sars cov
- respiratory syndrome coronavirus
- coronavirus disease
- angiotensin converting enzyme
- immune response
- endothelial cells
- angiotensin ii
- risk factors
- oxidative stress
- venous thromboembolism
- dendritic cells
- intensive care unit
- atrial fibrillation
- early onset
- toll like receptor
- vascular endothelial growth factor
- inflammatory response
- cell therapy
- bone marrow
- drug induced
- binding protein